science

Selected copper(I) complexes as potential

anticancer agent
Micha POTEK, Karol DUDEK, Agnieszka KYZIO Jagiellonian University in Krakow, Poland
Please cite as: CHEMIK 2013, 67, 12, 11811190

Introduction
Cancer is the second most frequent cause of death in the world
[1]. The discovery of antitumor activity of cisplatin began a search
for other metal complexes with cytotoxic properties against
cancer cells. One of the transition metal, whose complexes are
extensively tested for antitumor application is copper. Copper is
a trace element essential for human life. It is a building element of
several important enzymes (e.g. superoxide dismutase, cytochrome
oxidase, tyrosinase) and it regulates the intracellular redox potential,
while its complexes possess antibacterial, antifungal, antiviral, antiinflammatory and anticancer properties. As potential anticancer
drugs, there are currently extensively studied mainly complexes
of copper(II). There are only few complexes of copper(I) in the
literature, whereas they also show a very strong cytotoxic activity
against tumor cells in vitro [2].

covalently bound to DNA. In this form, it was oxidized to a copper(II)

compound in the presence of hydrogen peroxide. The final result of
those processes was cutting DNA or RNA strands into fragments.
The postulated factor directly responsible for cutting the DNA
was an adduct in which [Cu(phen)2]2+ was coordinated with the
hydroxyl radical OH and linked by non-covalent interactions
with DNA [7, 8].
Copper compounds coordinated to phenanthroline skeleton
ligands (see Fig. 1), such as [Cu(dmp)2]+, are thought to have the ability
of intercalation. Furthermore, it was indicated that the [Cu(dmp)2]+
(dmp=2,9-dimethyl-1,10-phenanthroline) can be an inhibitor of the
process of DNA transcription [9]. The [Cu(bcp)2]+ (bcp=2,9-dimethyl4,7-diphenyl-1,10-phenanthroline) is in turn believed to possess the
ability of forming bridges between double-stranded fragment of DNA
and another fragment of such a type [10].

Anticancer activity of copper

Over 95% of copper (both Cu(II) and Cu(I)) that is present
in serum is bound to ceruloplasmin (ferroxidase). However, it is
not responsible for transporting copper inside the cell. Before they
enter the cell, copper(II) ions are reduced to copper(I) by metaloreducatases located on the cells surface. Cu+ ions are transported
into the cell mainly by a specific copper transporter (hCtr). The
independent system of entering the cell, enables biologically active
copper compounds to penetrate the cell surface without binding
to other agents as opposite to coordination compounds of other
metals [24].
Anticancer activity of copper(I) compounds may be a result of
different mechanisms. They are described in the following paragraphs
of this review.
Anticancer activity of copper complex compounds is related
to their ability to produce reactive oxygen species (ROS). Copper(I)
ions can reduce hydrogen peroxide to hydroxyl radical. Copper(II)
ions may in turn be reduced to Cu(I) by superoxide anion(O2-),
or glutathione. Therefore, it can be concluded that the production
of reactive oxygen species such as OH are driven by the copper,
regardless of the form in which it is initially introduced into the body
Cu+, or Cu2+ [2, 5].

Selected cuprous complexes

Selected complexes of copper(I), which were extensively
investigated for anticancer activity, are presented in the subsequent
paragraphs. Diversity of ligands used to synthesize those complexes
causes that each one could possess other mechanism of action.

Cu2+ + O2 Cu+ + O2
Cu+ + H2O2 Cu2+ + OH + OH
Superoxide anion (O2-) is the product of reduction of the
molecular oxygen that occurs in many biological processes. It is
converted into hydrogen peroxide through dismutation. Both
of these forms of ROS lead to the formation of another type of
reactive oxygen species the hydroxyl radical (OH). It occurs
in a reaction catalysed by copper (or iron) ions. This radical is
believed to be the main factor causing DNA damage in cells under
oxidative stress [6].
Copper compounds are also thought to have nuclease activity.
The ability of copper to cut a DNA helix has been proved in studies
conducted with the use of Cu(I) complexes with two molecules
of 1,10-phenanthroline (phen). [Cu(phen)2]+ was initially non-

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Mononuclear compounds
In 1987 Berners-Price and co-workers [11] presented copper(I)
complexes with molecular formula [Cu(P-P)2]Cl, where central Cu+
ion was coordinated with two molecules of bidentate phosphine. The
structures of these complexes are presented in Figure 1.

Fig. 1. The structures of copper(I) complexes with bidentate phosphine

Cytotoxicity of compounds 1B and 1C are several times higher than

the one presented by uncoordinated ligands tested in the same cell line.
Compound 1D possesses anticancer activity (only in vitro), however
it is lower than in 1B and 1C. Moreover, 1C also possesses in vivo
anticancer activity. Additionally, the equilibrium between mononuclear
[Cu(dppe)2]Cl and binuclear form (CuCl)2(dppe)3 is observed in 1A
solution. For this reason cytotoxicity cannot be unambiguously assigned
to mononuclear [Cu(dppe)2]Cl [11].
In order to increase solubility of copper(I) complexes in
water, Marzano et al. introduced the hydroxyl groups to analysed
phosphines. It is worth to mention that introduction of OH does not
destabilize cuprous complexes. Structure of copper(I) complex ion
of compound [Cu(thp)4][PF6] (2), synthesized by the same research
group, is shown in Figure 2. In this compound central ion Cu+ is
coordinated with four molecules of tris(hydroxymethyl)phosphine.

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Fig. 2. Complex ion of the compound [Cu(thp)4][PF6]

[Cu(thp)4][PF6] exhibits even 40-fold higher cytotoxicity than

cisplatin (e.g. for colorectal adenocarcinoma cell line CaCo-2:
IC50 =1.08 0.12 M for 2, IC50 = 35.42 1.40 M for cisplatin;
48-hours test) [12]. Moreover, in survey performed on cancer cells
of a colon 2 reacts selectively with cancer cells, but at the same
time it is not harmful for healthy cells. The selectivity is higher than
the one observed at cisplatin or oxaliplatin the drug applied in
colorectal cancer treatment (e.g. for non-tumour human fibroblasts
cell line MRC-5: IC50 = 32.67 1.34 M for 2, IC50 = 19.66 1.31
M for cisplatin and IC50 =23.93 1.35 M for oxaliplatin; 72-hours
test) [13]. What is more, this compound is effective in case of those
types of cancer which are resistant to platin complexes (e.g. for
colon carcinoma cell line LoVo IC50=2.05 0.43 M for oxaliplatin,
1.37 0.35 M for compound 2, whereas for resistant to oxaliplatin
cell line LoVo-OxPt IC50=10.89 1.34 M for oxaliplatin and
IC50=1.46 0.27 M for 2; 48-hours assay) [13]. The described
complex of copper leads to cell death via nonapoptotic way (so-called
type III cell death). Cell death is not caused by DNA fragmentation.
What is more, activation of caspases does not take place. On the
contrary, 2 may even inhibit caspases 3 and 7. Characteristic of
this type of cell death are: massive cytoplasmic vacuolization,
endoplasmic reticulum stress and inhibition of proteasome 26S
functions. Furthermore, an increased production of reactive oxygen
species (ROS) was observed, which caused an oxidative stress and
led cells to death. It was unexpected that the complex [Cu(bhpe)2]
[PF6] synthesized by the same research group (Fig. 3), where
monodentate phosphines were replaced by bidentate phosphines,
would show only an inconsiderable anticancer activity. It was much
lower not only than 2, but also than cisplatin (e.g. for colorectal
adenocarcinoma cell line CaCo-2: IC50 = 52.50 0.81 M for 3,
IC50 = 1.08 0.12 M for 2, IC50 = 35.42 1.40 M for cisplatin;
48-hours test) [12].
The reason for an insignificant cytotoxicity of compound 3 could
be its high stability and inertness in process of ligands exchange. It
could be confirmed by results obtained from a mass spectrometry.
For complex 3 no fragmentation was observed, as opposed to 2, in
whose spectrum not only [Cu(thp)4]+ ion peak was observed, but also
peaks ascribed to [Cu(thp)3]+ and [Cu(thp)2]+. It can be concluded that
ability to exchange ligands has crucial influence for cytotoxicity of the
described complexes [12,13].

Fig. 3. Complex ion of compound [Cu(bhpe)2][PF6]

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Fig. 4. Complexes of Cu+ with triazolylborate ligands

These compounds present activity higher than the one observed

at cisplatin for all cell lines tested (Tab. 1), especially for lung adenocarcinoma cells (A549 cell line), where the IC50 value was approximately 17-fold lower for compound 4B (IC50 = 2.35 0.9 M) and
26-fold lower for complex 4A (IC50=1.52 0.7 M), than for tested
in the same condition cisplatin (IC50=39.27 1.9 M; 48-hours test)
[14]. The mechanism of the action has been unknown so far. However, it is posited that it could be similar to that exhibited by copper(I)
complex showed in Figure 5.

Fig. 5. Complex of Cu(I) leading to cell death in a nonapoptotic way

Compound 5 exhibits activity from 2 to 19 times higher than

cisplatin for investigated cell lines (e.g. for breast cancer cell line
MCF-7 IC50=1.55 0.19 M for 5 and IC50 = 30.18 1.5 M for
cisplatin; 48-hours test) [15]. In vitro tests suggest that the complex
mentioned leads to cell death in a nonapoptotic pathway, as it was
observed at[Cu(thp)4][PF6] (2). Lack of caspase 3 activity, an increase in
a cell size and a cytoplasmic vacuolization confirm this hypothesis [15].
Other interesting compound revealing much higher cytotoxicity
than cisplatin is a coordination compound of copper(I) displayed in
Figure 6 (e.g. for colon carcinoma cell line HCT-15 IC50=1.05 0.31 M
for 6 and IC50 = 16.65 2.63 M for cisplatin) [16].

Fig. 6. Electrically neutral copper(I) complex

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Anticancer activity is exhibited by copper(I) complexes possessing

pyridine-type ligands (pyridine, bipyridine, phenanthroline ect.),
or such where copper(I) ion is coordinated to phosphine ligands.
Presumably, introduction of both types of ligands mentioned to one
molecule would make it possible to create a compound with an
increased activity against cancer cells. Marzano research group,
mentioned before, synthesized complexes depicted in Figure 4,
which contained triazolylborate ligands.

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Due to the fact that the applied tridentate ligand simultaneously

neutralizes positive charge of Cu+ ion, the received compound 6 is
electrically neutral. A mechanism of cellular internalization has not been
explained so far. It is assumed that penetration of a cell membrane is not
supported by human copper transporters (hCtr), which can transfer
positively charged molecules. As the authors postulate, a dentate
ligand could be the factor, which supports complexes transfer. It acts
as ionophore, as it was the case with copper(II) complexes [16, 17].
Coordination number 4 is not the only one possible coordination
number for copper(I) complexes. In Figure 7 a two-coordinated
compound of Cu+ is depicted. In vitro cytotoxic activity of the presented
compound was approximately 2,5-fold higher than the one measured
for cisplatin. What is remarkable, this effect was also observed for cell
lines resistant to cisplatin (e.g. for sensitive to cisplatin human ovarian
cancer cell line 2008 IC50 = 1.84 0.32 M for 7 and 3.12 1.03
M for cisplatin; in case of resistant to cisplatin human ovarian cancer
cell line C13* IC50 is 2.08 0.72 for 7 and 22.18 2.01 for cisplatin;
72-hours assay) [18]. Presumably, mechanism of activity of compound 8
is connected with its confirmed ability to disturb respiration by altering
mitochondrial membrane potential and producing reactive oxygen
species [18].
Fig. 9. Binuclear copper(I) complexes synthesized by Balakrishna et al

Fig. 7. Two-coordinated complex of Cu(I)

Starosta et al. [1924] synthesized copper(I) complexes, whose

general structure is displayed in Figure 8.

Fig. 8. General structure of copper(I) complexes containing

phosphine, phenanthroline-type ligand and iodide ion

The obtained complexes show high cytotoxicity not only to human

ovarian carcinoma cell lines sensitive to cisplatin, but also to those
resistant to this drug (for resistant to cisplatin human ovarian carcinoma
cell line SKOV 3 IC50 is approximately 23 M depending on examined
copper(I) compounds, whereas for cisplatin IC50 = 180.5 9.3 M;
for sensitive to cisplatin human ovarian carcinoma cell line MDAH
2774 IC50 is approximately 27 M for analysed copper(I) complex and
77.27.6 M for cisplatin; 24-hours test) [19]. As the authors proved,
activity exhibited by investigated cuprous compound is many times
higher than the one presented by uncoordinated diimine or phosphine
ligands (IC50:100500 M in case of both cell lines: SKOV 3 and MDAH
2774) [1924].
Polinuclear compounds
In 2010 Balakrishna and co-workers [25] exhibited group of
polinuclear copper(I) complexes, which possessed in their coordination
sphere both pyridine-type and phospine-type ligands. In Figures 9 and
10 examples of synthesized compounds are depicted.
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Fig. 10.Octanuclear Cu+ compound synthesized by Balakrishna et al

Antiproliferative activity for cervical cancer cells was proved

for all three copper complexes presented in Figures 10 and 11.
Moreover, it was observed that inhibition of proliferation was more
effective for the complexes discussed, than for cisplatin, especially
for 9B (antiproliferative ability was assessed as a percent of inhibition
of cervical cancer HeLa cell line proliferation: 50 4 % for 9A,
62 9 % for 10, 100 % for 9B and 49 7 % for cisplatin; in
10 M concentration) [25]. Biological tests carried out with the use of
this complex show that 9B inhibits proliferation not only of cervical
cancer cells, but also of human breast cancer cells and Chinese
hamster ovary cells. Moreover, it is several times more efficient
than cisplatin. Furthermore 9B has an ability to damage the DNA
integration, block cell cycle in G1 phase and induce apoptosis [25].
Another interesting binuclear cuprous compound revealing
anticancer activity, is depicted in Figure 12 complex with formula
[Cu2(dppe)3(CH3CN)4](ClO4).

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Cu(I)
compound

Lit.

probably DNA damages,

single-strand breaks in
supercoiled plasmid-DNA
in vitro

11

A549 (lung carcinoma)

MCF-7 (breast carcinoma)
HepG2 (liver carcinoma)
CaCo-2, HCT-15, LoVo , DLD1,
SW480 (colon cancer)
HeLa (cervix carcinoma)
A375 ( melanoma)
Daudi (Brukitt lymphoma)
HL60 (promyelocytic leukemia)

strong antiproliferative
activity
reactive oxygen species
production
nonapoptotic cell death
(inhibitionof caspases
3 and 7) - cytoplasmic
vacuolization, endoplasmic
reticulum stress, proteasome
26S inhibition)

12
13

4A, 4B

A549 (lung adenocarcinoma)

A375 ( melanoma)
HL60 (promyelocytic leukemia)
A431 (cervix cancer)
2008 (ovarian cancer)

changes in redox potential

of cell membrane which is
the result of disruption in
oxidative phosphorylation
process

14

A549 (lung carcinoma)

HL60 (promyelocytic leukemia)
MCF-7 (breast carcinoma)
A375 (melanoma)
LoVo (colon carcinoma)

nonapoptotic cell death

(caspase-3 activity was
not observed, cytoplasmic
vacuolisation and increase in
cell size)

15

mechanism still unknown

MCF-7 (breast carcinoma)
ligand acts as ionophore
A549 (lung carcinoma)
A375 ( melanoma)
HL60 (promyelocytic leukemia)
HCT-15, LoVo (colon carcinoma)
A431 (cervix cancer)
2008, C13* (ovarian cancer)

HL60 (promyelocytic leukemia)

MCF-7 (breast cancer)
HCT-15 (colon carcinoma)
HeLa (cervix carcinoma)
A549 (lung carcinoma)
2008, C13* (ovarian cancer)

ability to disturb respiration

by altering mitochondrial
membrane potential and
producing reactive oxygen
species

SKOV 3, MDAH 2774 (human

ovarian carcinoma)

mechanism unknown

Fig. 11. [Cu2(dppe)3(CH3CN)4](ClO4)2

Summary
Mechanisms of anticancer activity discussed in this article are
presented on Scheme 1. Copper(I) coordination compounds described
in this review are in turn collected in Table 1. It summarises their biological
activity and types of cell line, in which complexes were tested in vitro.
Copper(I) compounds may become an alternative for cisplatin,
which possesses a few drawbacks but is still most popular. Copper, as an
essential element for human life is supposed to be less toxic than other
metals, like platinum or ruthenium, analysed for medical application.
Both copper ions, Cu+ and Cu2+ can induce oxidation stress via catalysis
and production of reactive oxygen species. Superiority of copper(I)
compounds over copper(II) compounds results from nuclease activity of
Cu+ complexes and selectivity exhibited by human copper transporters
(hCtr) in introduction of Cu+ ions to cells. Copper as an antibacterial
agent is used in hospitals, health centres and public buildings for various
sanitary applications (for instance handles, holders, handrails ect.) [28].
As it was presented in this article, copper(I) coordination compounds
have remarkable application potential. Intensive research may enable
to finally apply them as anticancer drugs.

Biological activity

P388 (mouse leukemia)

B16 (melanoma)
M5076 (reticulum cell sarcoma)

1C

The anticancer activity of compound 11 was confirmed by tests

carried out on several cell lines (Table 1) [26]. 11 managed to damage
DNA helix, inhibit processes of its synthesis, stop cell cycle in G1 and
G2 phases and induce apoptosis. If 11 and adriamycin (drug in cancer
therapy) are used simultaneously in treatment, synergism of action is
observed. 11 increases therapeutic effect of adriamycin and vice versa.
It is believed that 11 binds to DNA by displacement of acetonitrile
molecules. Simulations with a use of molecular modelling methods imply
that the most profitable donor of a pair of electrons is the atom N7
of guanine. Since in one molecule of 11 two Cu+ ions are present, the
discussed copper(I) complex acts as chelate agent. It creates two bonds
with DNA, as a result of replacement of two acetonitrile molecules for
two guanine molecules of deoxyribonucleic acid. Mutual strengthening
of anticancer activity between 11 and adriamycin suggests that both
agents bind to other helix regions. Moreover each one causes changes
in DNA in a way that facilitates binding of the second one [27].

Cancer cell line, in which

investigations were performed

9A, 10

9B

HeLa (cervical cancer)

16

1924

antiproliferative activity

25

antiproliferative activity
HeLa (cervical cancer)
MCF-7 and MDA-MB 231 (breast ability to damage DNA
integrity
cancer)
CHO (Chinese hamster ovarian inhibition of cell cycle in G1
phase
cancer)
induction of apoptosis
H460 (lung cancer)

11

18

DNA damages
DNA synthesis inhibition
inhibition of cell cycle in G1
phase
induction of apoptosis
synergetic enhancement
of activity when it is
used simultaneously with
adriamycin

25

26
27

Literature

Scheme 1. Selected examples of anticancer activity and mode

of action of Cu(I) complexes

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Table 1

Biological activity of described cuprous complexes

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Micha POTEK M.Sc., graduated from the Faculty of Chemistry

of the Jagiellonian University (2012). Currently, he is a Ph.D. student of
Coordination and Bioinorganic Physicochemistry Group of Jagiellonian
University. He works on synthesis and characteristics of coordination
compounds with a potential biological application. Moreover he works at
Inter-Academy Institute of Conservation and Restoration of Works of Art
(Warsaw-Cracow).
e-mail: michalplotek@gmail.com

Karol DUDEK - M.Sc., graduated from the Faculty of Chemistry of

the Jagiellonian University (2012). Currently, he is a Ph.D. student in the
Department of Chemical Education JU. He deals with implementation of
IBSE in Polish educational system and he examines the role of learning
through inquiry in the development of chemical skills. He also teaches
in Private Academic Secondary School No 8 of Krakw and in Private
Primary School Academos.

Agnieszka KYZIO - Ph.D., graduated from the Faculty of Chemistry of the Jagiellonian University (2002). In 2007 she received her
PhD degree in Chemistry. She is currently an assistant professor in the
Coordination and Bioinorganic Physicochemistry Group at the Faculty
of Chemistry UJ. Her main interests and research work are focused on
metal complexes and biomaterials with potential biological activity for
medical applications (anticancer therapies, antimicrobial agents). She is
co-author of over 20 scientific publications and numerous conference
presentations.

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